期刊
BIOMOLECULES & THERAPEUTICS
卷 28, 期 5, 页码 381-388出版社
KOREAN SOC APPLIED PHARMACOLOGY
DOI: 10.4062/biomolther.2020.044
关键词
Methamphetamine; Neurotoxicity; Neuroinflammation; Excitotoxicity; Apoptosis
资金
- Basic Science Research Program through National Research Foundation of Korea (NRF) - Ministry of Education [NRF-2016R1A6A1A03011325]
- Keimyung University
- National Research Foundation of Korea [5120200313763] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Methamphetamine (METH) is a highly addictive psychostimulant and one of the most widely abused drugs worldwide. The continuous use of METH eventually leads to drug addiction and causes serious health complications, including attention deficit, memory loss and cognitive decline. These neurological complications are strongly associated with METH-induced neurotoxicity and neuroinflammation, which leads to neuronal cell death. The current review investigates the molecular mechanisms underlying METH-mediated neuronal damages. Our analysis demonstrates that the process of neuronal impairment by METH is closely related to oxidative stress, transcription factor activation, DNA damage, excitatory toxicity and various apoptosis pathways. Thus, we reach the conclusion here that METH-induced neuronal damages are attributed to the neurotoxic and neuroinflammatory effect of the drug. This review provides an insight into the mechanisms of METH addiction and contributes to the discovery of therapeutic targets on neurological impairment by METH abuse.
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